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10.1089/ars.2013.5828 http://scihub22266oqcxt.onion/10.1089/ars.2013.5828 C4224049!4224049!24787605     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Antioxid+Redox+Signal 2014 ; 21 (16): 2231-45 Nephropedia Template TP {{tp|p=24787605|t=2014. Reactive Oxygen Species Deficiency Induces Autoimmunity with Type 1 Interferon Signature |pdf=|usr=}}{{24787605}} gab.com Text Reactive Oxygen Species Deficiency Induces Autoimmunity with Type 1 Interferon Signature JO: Antioxid Redox Signal http://www.kidney.de/pget.php?&tw=1&pmid=24787605 #FOAvip Aims: Chronic granulomatous disease (CGD) is a primary immunodeficiency caused by mutations in the phagocyte reactive oxygen species (ROS)?producing NOX2 enzyme complex and characterized by recurrent infections associated with hyperinflammatory and autoimmune manifestations. A translational, comparative analysis of CGD patients and the corresponding ROS-deficient Ncf1m1J mutated mouse model was performed to reveal the molecular pathways operating in NOX2 complex deficient inflammation. Results: A prominent type I interferon (IFN) response signature that was accompanied by elevated autoantibody levels was identified in both mice and humans lacking functional NOX2 complex. To further underline the systemic lupus erythematosus (SLE)-related autoimmune process, we show that naïve Ncf1m1J mutated mice, similar to SLE patients, suffer from inflammatory kidney disease with IgG and C3 deposits in the glomeruli. Expression analysis of germ-free Ncf1m1J mutated mice reproduced the type I IFN signature, enabling us to conclude that the upregulated signaling pathway is of endogenous origin. Innovation: Our findings link the previously unexplained connection between ROS deficiency and increased susceptibility to autoimmunity by the discovery that activation of IFN signaling is a major pathway downstream of a deficient NOX2 complex in both mice and humans. Conclusion: We conclude that the lack of phagocyte-derived oxidative burst is associated with spontaneous autoimmunity and linked with type I IFN signature in both mice and humans. Antioxid. Redox Signal. 21, 2231?2245. Twit Text FOAVip Reactive Oxygen Species Deficiency Induces Autoimmunity with Type 1 Interferon Signature ????Antioxid Redox Signal http://www.kidney.de/pget.php?&tw=1&pmid=24787605 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24787605 #FOAvip English Wikipedia <ref>{{Cite pmid|24787605}}</ref> Reactive Oxygen Species Deficiency Induces Autoimmunity with Type 1 Interferon Signature #MMPMID24787605 Kelkka T; Kienhöfer D; Hoffmann M; Linja M; Wing K; Sareila O; Hultqvist M; Laajala E; Chen Z; Vasconcelos J; Neves E; Guedes M; Marques L; Krönke G; Helminen M; Kainulainen L; Olofsson P; Jalkanen S; Lahesmaa R; Souto-Carneiro MM; Holmdahl R Antioxid Redox Signal 2014[Dec]; 21 (16): 2231-45 PMID24787605show ga Aims: Chronic granulomatous disease (CGD) is a primary immunodeficiency caused by mutations in the phagocyte reactive oxygen species (ROS)?producing NOX2 enzyme complex and characterized by recurrent infections associated with hyperinflammatory and autoimmune manifestations. A translational, comparative analysis of CGD patients and the corresponding ROS-deficient Ncf1m1J mutated mouse model was performed to reveal the molecular pathways operating in NOX2 complex deficient inflammation. Results: A prominent type I interferon (IFN) response signature that was accompanied by elevated autoantibody levels was identified in both mice and humans lacking functional NOX2 complex. To further underline the systemic lupus erythematosus (SLE)-related autoimmune process, we show that naïve Ncf1m1J mutated mice, similar to SLE patients, suffer from inflammatory kidney disease with IgG and C3 deposits in the glomeruli. Expression analysis of germ-free Ncf1m1J mutated mice reproduced the type I IFN signature, enabling us to conclude that the upregulated signaling pathway is of endogenous origin. Innovation: Our findings link the previously unexplained connection between ROS deficiency and increased susceptibility to autoimmunity by the discovery that activation of IFN signaling is a major pathway downstream of a deficient NOX2 complex in both mice and humans. Conclusion: We conclude that the lack of phagocyte-derived oxidative burst is associated with spontaneous autoimmunity and linked with type I IFN signature in both mice and humans. Antioxid. Redox Signal. 21, 2231?2245. äReactive Oxygen Species Deficiency Induces Autoimmunity with Type 1 In(epmc).pdf DeepDyve Pubget Overpricing